Formation of plaque is the result of fat deposits and calcium compound deposits such as cholesterol and hydroxyapatite --C.sub.a5 (PO.sub.4).sub.3 OH-- in the arterial wall, between the intima and the lumina. Whenever a serious stenosis is present, the patient complains of chest pain during stress and there is a significant risk of heart disease.
In the majority of cases, this narrowing in the coronary artery can be dilated by percutaneous angioplasty, using a manual pressure inflator. The duration of balloon inflation is, at the present time, arbitrarily defined by the operator or limited by the severity of ischemic paincaused by the inflated balloon. The early complication of this method is arterial dissection and possible occlusion, caused by the uncontrolled manual inflation of the balloon.
The injury to the arterial wall caused by the balloon may enhance growth factor secretion and induce smooth muscle cell proliferation and extra cellular matrix deposition, thus causing restenosis. The restenosis usually appears within six months after angioplasty in about 30% to 50% of the patients, thus limiting the efficacy of this procedure. Many patients will need recatheterization, repeat angioplasty and coronary bypass operations.
In most cases, the narrowed lumen is dilated by the known angioplasty method, whereby the balloon is inflated by a manual inflator pump and applies substantial mechanical pressures (e.g., 8-10 Atm.) during dilation. Since the mechanical pressure is manually increased, the pressure delivery by this method is not accurately controlled and is carried out in a relatively too short time, without any interdependence of the pressure in time. The time period of the balloon inflation is randomly determined by the performing surgeon or by the ability of the patient to endure the ischemic pains caused by the inflated balloon. In the manual method used today, the dissection of the artery is frequent, causing extensive damage to the artery, which in turn may cause acute total occlusion of the artery and may subject the patient to myocardial infarction and, on some occasions, even to restenosis.
U.S. Pat. No. 5,152,776 discloses a balloon inflation device in which the pressure monitor 70 is connected in the device between the motor 45 of the drive mechanism and the pump means 50. Both the motor 45 as operated by the drive mechanism and the pressure monitor 70 are controlled by a microprocessor unit 90. Contrary to this arrangement, according to the present invention a pressure sensor transducer is advantageously directly connected to the input of the balloon, namely, between the inflator pump and the balloon. Signals from the transducer are constantly measured and the data is conveyed to a processor and control unit. Should the pressure in the balloon suddenly rise, the control unit immediately stops the procedure. Similarly, if the pressure in the balloon drops, for example, a pressure drop caused by a leak in the balloon, rapid deflation of the balloon is effected, thus preventing further inflation and fluid leakage through the ruptured balloon.
It is therefore a broad object of the present invention to ameliorate the disadvantages of the manually operated, balloon inflator, as well as the disadvantages of the microprocessor controlled balloon inflation devices, and to provide a pressure sensing and activating control system for the performance of CAPSAD.
It is a further object of the invention to provide a, method for dilating a section of an elastic conduit by means of an inflatable balloon inserted therein, which method reduces the danger of dissection of the conduit and increases the chances of preventing collapse of the conduit after a period of time.